Exosomal MicroRNAs Released by Activated Astrocytes as Potential Neuroinflammatory Biomarkers

Int J Mol Sci. 2020 Mar 27;21(7):2312. doi: 10.3390/ijms21072312.

Abstract

Neuroinflammation is a hallmark of several neurodegenerative diseases and disorders, including traumatic brain injury (TBI). Neuroinflammation results in the activation of glial cells which exacerbates the neuroinflammatory process by secretion of pro-inflammatory cytokines and results in disruption of glial transmission networks. The glial cells, including astrocytes, play a critical role in the maintenance of homeostasis in the brain. Activated astrocytes release several factors as part of the inflammatory process including cytokines, proteins, and microRNAs (miRNAs). MiRNAs are noncoding RNA molecules involved in normal physiological processes and disease pathogenesis. MiRNAs have been implicated as important cell signaling molecules, and they are potential diagnostic biomarkers and therapeutic targets for various diseases, including neurological disorders. Exosomal miRNAs released by astrocytic response to neuroinflammation is not yet studied. In this study, primary human astrocytes were activated by IL-1β stimulation and we examined astrocytic exosomal miRNA cargo released in a neuroinflammatory stress model. Results indicate that acute neuroinflammation and oxidative stress induced by IL-1β generates the release of a specific subset of miRNAs via exosomes, which may have a potential role in regulating the inflammatory response. Additionally, these miRNAs may serve as potential biomarkers of neuroinflammation associated with neurological disorders and injuries.

Keywords: Astrocytes; Biomarkers; MicroRNA; neuroinflammation.

MeSH terms

  • Astrocytes / metabolism*
  • Biomarkers / metabolism*
  • Brain / metabolism
  • Brain Injuries, Traumatic / metabolism
  • Cytokines / metabolism
  • Exosomes / metabolism*
  • Homeostasis
  • Humans
  • Inflammation / metabolism*
  • Interleukin-1beta / metabolism*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neurodegenerative Diseases / metabolism
  • Neuroglia / metabolism
  • Oxidative Stress
  • Signal Transduction

Substances

  • Biomarkers
  • Cytokines
  • IL1B protein, human
  • Interleukin-1beta
  • MicroRNAs